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Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients
J Blauensteiner1, R Bertinat2, L E León3
1Institute of Biomedical Science, Department of Health Studies, FH Joanneum University of Applied Sciences, Graz, Austria.
Abstract:
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease characterized by unexplained debilitating fatigue. Although the etiology is unknown, evidence supports immunological abnormalities, such as persistent inflammation and immune-cell activation, in a subset of patients. Since the interplay between inflammation and vascular alterations is well-established in other diseases, endothelial dysfunction has emerged as another player in ME/CFS pathogenesis. Endothelial nitric oxide synthase (eNOS) generates nitric oxide (NO) that maintains endothelial homeostasis. eNOS is activated by silent information regulator 1 (Sirt1), an anti-inflammatory protein. Despite its relevance, no study has addressed the Sirt1/eNOS axis in ME/CFS. The interest in circulating microRNAs (miRs) as potential biomarkers in ME/CFS has increased in recent years. Accordingly, we analyze a set of miRs reported to modulate the Sirt1/eNOS axis using plasma from ME/CFS patients. Our results show that miR-21, miR-34a, miR-92a, miR-126, and miR-200c are jointly increased in ME/CFS patients compared to healthy controls. A similar finding was obtained when analyzing public miR data on peripheral blood mononuclear cells. Bioinformatics analysis shows that endothelial function-related signaling pathways are associated with these miRs, including oxidative stress and oxygen regulation. Interestingly, histone deacetylase 1, a protein responsible for epigenetic regulations, represented the most relevant node within the network. In conclusion, our study provides a basis to find endothelial dysfunction-related biomarkers and explore novel targets in ME/CFS.
Insights
This study found increased levels of specific microRNAs (miRs) in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), suggesting a role for endothelial dysfunction in the disease. These findings may help identify new biomarkers and therapeutic targets for ME/CFS.
Area of Science:
- Immunology
- Vascular Biology
- Biomarker Discovery
Background:
- Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex illness with unknown causes, but immunological abnormalities and inflammation are implicated.
- Endothelial dysfunction, involving the Sirt1/eNOS pathway, is a potential factor in ME/CFS pathogenesis.
- MicroRNAs (miRs) are increasingly recognized as potential biomarkers for complex diseases.
Purpose of the Study:
- To investigate the Sirt1/eNOS axis in ME/CFS by analyzing specific microRNAs (miRs) in patient plasma.
- To identify potential circulating biomarkers related to endothelial dysfunction in ME/CFS.
Main Methods:
- Analysis of plasma microRNA levels (miR-21, miR-34a, miR-92a, miR-126, miR-200c) in ME/CFS patients and healthy controls.
- Examination of public microRNA data from peripheral blood mononuclear cells.
- Bioinformatics analysis to identify associated signaling pathways and regulatory networks.
Main Results:
- Five specific microRNAs (miR-21, miR-34a, miR-92a, miR-126, miR-200c) were found to be significantly elevated in ME/CFS patients compared to controls.
- Similar increases in these miRs were observed in public datasets of peripheral blood mononuclear cells.
- Bioinformatics analysis linked these miRs to endothelial function, oxidative stress, and oxygen regulation pathways, with histone deacetylase 1 identified as a key regulatory node.
Conclusions:
- The study identifies a set of microRNAs associated with endothelial dysfunction in ME/CFS.
- These findings provide a foundation for developing novel biomarkers for ME/CFS.
- The identified microRNAs and regulatory pathways represent potential therapeutic targets for ME/CFS.
